【24h】

Cue-elicited drug craving represses ERK activation in mice prefrontal association cortex.

机译:提示引起的药物渴望抑制了小鼠前额叶皮层的ERK活化。

获取原文
获取原文并翻译 | 示例
获取外文期刊封面目录资料

摘要

Morphine addiction is characterized by compulsive drug-taking behavior and high rates of relapse that reflect reward-controlled learning, consolidation and reconsolidation of drug cues. Extracellular signal-regulated protein kinase (ERK) is one of the cellular molecules that have been highly implicated in the synaptic plasticity processes of learning and memory in cocaine addiction. However, the roles of ERK in the morphine-paired conditioned place preference (CPP) are not clear. In the present study, we found that compared to the morphine-unpaired and saline-paired and saline-unpaired groups, morphine-paired mice showed depressed ERK2 activity in the Frontal Association Cortex (FrA), whereas ERK1 activity was not changed in the same region. In the Accumbens Nucleus (Acb) and Caudate Putamen (CPu) that are associated with cocaine addiction, the activities of ERK1 and ERK2 among four groups showed no difference. These results suggest that the FrA plays an important role in morphine craving and that ERK2 is involved in eliciting the environment-related morphine craving, which is totally different from those induced by morphine itself.
机译:吗啡成瘾的特征在于强迫性的吸毒行为和高复发率,这反映了奖励控制的学习,药物线索的巩固和再巩固。细胞外信号调节蛋白激酶(ERK)是可卡因成瘾中与学习和记忆的突触可塑性过程高度相关的细胞分子之一。但是,ERK在吗啡配对条件化位置偏好(CPP)中的作用尚不清楚。在本研究中,我们发现与吗啡未配对,生理盐水配对和生理盐水未配对的组相比,吗啡配对的小鼠在额叶皮质(FrA)中显示出ERK2活性降低,而ERK1活性在相同的条件下没有变化地区。在与可卡因成瘾有关的伏隔核(Acb)和尾状壳蛋白(CPu)中,四组中ERK1和ERK2的活性没有差异。这些结果表明,FrA在吗啡渴望中起重要作用,而ERK2参与引起与环境有关的吗啡渴望,这与吗啡本身引起的完全不同。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号